Weitere Antikörper gegen CCL20 Interaktionspartner

Hypoxia is a transcriptional inducer of CCL20 in human mononuclear phagocytes.

Human Chemokine (C-C Motif) Ligand 20 (CCL20) Interaktionspartner

CCL20, which is regulated by HuR and secreted into the bone microenvironment, enhances the metastatic ability and bone metastasis of breast cancer cells by stimulating cancer cells and osteoblastic cells in both autocrine and paracrine manners.

CCL20 may play an important role in the pathogenesis of MS. Both allelic variation of (rs6749704) within CCL20 gene and (rs763780) within IL-17F gene can be considered risk factor for development of MS in Egyptian patients.

These results provide evidence that necrotic cells induce the expression of CCL2/MCP-1 and CCL20/MIP-3alpha in glioblastoma cells through activation of NF-kappaB and AP-1 and facilitate the infiltration of microglia into tumor tissues.

CCN1 stimulates CCL20 production in vitro and in vivo, and thus supports the notion that overexpressed CCN1 in hyperproliferating keratinocyte is functionally involved in the recruitment of inflammatory cells to skin lesions affected by psoriasis.

There was underexpression of the majority of genes after sunitinib treatment. The lower expression levels of IGFBP1, CCL20, CXCL6 and FGB were confirmed by qRT-PCR in all cases. The downregulation of gene expression leads us to search for methylation as a mechanism of action of the tyrosine kinase inhibitors

High expression of CCL20 is associated with cutaneous T-cell lymphoma.

These results showed that the higher levels of CXCL10, CCL20 and CCL22 were associated with ischemic heart disease. The serum levels of chemokines may influence by the certain traditional risk factors of IHD and some studied SNPs, but did not influence by treatment and gender of patients.

The strongest OR was for CXCL8 (interleukin-8) in serum (96.8, 95% CI: 11.9-790.2). Of these 15 markers, 6 were also significantly elevated in serum from Chile (CCL20, C-reactive protein, CXCL8, CXCL10, resistin, serum amyloid A).

Blocking or knockdown CCN1 expression ameliorated skin inflammation and reduced the expression of CCL20 in both imiquimod and IL-23-induced psoriasis-like mouse models.

these data indicate that CCL20/CCR6 signaling may play an important role in regulating bone mass accrual, potentially by modulating osteoblast maturation, survival, and the recruitment of osteoblast-supporting cells.

We crossed Ptf1a(Cre/+) ;Kras(G12D/+) mice with JNK1(-/-) mice to generate Ptf1a(Cre/+) ;Kras(G12D/+) ;JNK1(-/-) (Kras;JNK1(-/-) ) mice. Tumor weight was significantly lower in Kras;JNK1(-/-) mice than in Kras;JNK1(+/-) mice, whereas histopathological features were similar.we concluded that inhibition of activated JNK in pancreatic tumor stroma could be a potential therapeutic target to increase Ccl20 secretion

Taken together, these data show that, in adipose tissues, IL-17A contributes to exacerbating insulin resistance-enhancing IL-6 production and promotes the infiltration of Th17 cells in cooperation with TNFalpha; these findings represent a novel hypothesis for the association between IL-17A-producing cells and type 2 diabetes.

Data (including data from studies in knockout/mutant mice) suggest that expression of Ahr (aryl-hydrocarbon receptor) and its translocation into nucleus are necessary for Ahr ligand-mediated synergistic induction of Ccl20; here, TCDD is Ahr ligand.

alpha-hemolytic streptococcus may exacerbate kidney damage in IgA nephropathy through CCL20 response to the effect of Th17 cells.

Data indicate that a CCR6/CCL20 chemokine loop instructed rapid increase of B cells in the spleen in response to systemic administration of Nod1 agonists in a TNF-alpha-dependent manner.

Neutralization of CCL20 before induction of sepsis increased mortality during sepsis accompanied with increasing epithelial apoptosis in the jejunum and augmenting serum TNF-alpha.

CXCR3 promotes recruitment of Th17 cells from the blood into the liver in both human and murine liver injury. Their subsequent positioning near bile ducts is dependent on CCR6 and cholangiocyte-secreted CCL20.

Findings suggest that TNF-alpha is essential in the induction of autoimmune hepatitis (AIH) through upregulation of hepatic CCL20 expression, which allows migration of dysregulated splenic T cells.